Safety and efficacy of the 5-lipoxygenase-activating protein inhibitor AZD5718 in patients with recent myocardial infarction: The phase 2a FLAVOUR study.


Journal

International journal of cardiology
ISSN: 1874-1754
Titre abrégé: Int J Cardiol
Pays: Netherlands
ID NLM: 8200291

Informations de publication

Date de publication:
15 10 2022
Historique:
received: 21 06 2022
accepted: 12 07 2022
pubmed: 17 7 2022
medline: 30 8 2022
entrez: 16 7 2022
Statut: ppublish

Résumé

Leukotrienes are pro-inflammatory vasoactive lipid mediators implicated in the pathophysiology of atherosclerotic cardiovascular disease. We studied the effect of the 5-lipoxygenase-activating protein inhibitor AZD5718 on leukotriene biosynthesis and coronary microvascular function in a single-blind, phase 2a study. Patients 7-28 days after myocardial infarction (±ST elevation), with <50% left anterior descending coronary artery stenosis and Thrombolysis in Myocardial Infarction flow grade ≥ 2 after percutaneous coronary intervention, were randomized 2:1:2 to once-daily AZD5718 200 mg or 50 mg, or placebo, in 4- and 12-week cohorts. Change in urine leukotriene E Of 129 randomized patients, 128 received treatment (200 mg, n = 52; 50 mg, n = 25; placebo, n = 51). Statistically significant reductions in uLTE In patients with recent myocardial infarction, AZD5718 was well tolerated, and leukotriene biosynthesis was dose-dependently inhibited. No significant changes in CFVR were detected. gov identifier: NCT03317002.

Sections du résumé

BACKGROUND
Leukotrienes are pro-inflammatory vasoactive lipid mediators implicated in the pathophysiology of atherosclerotic cardiovascular disease. We studied the effect of the 5-lipoxygenase-activating protein inhibitor AZD5718 on leukotriene biosynthesis and coronary microvascular function in a single-blind, phase 2a study.
METHODS
Patients 7-28 days after myocardial infarction (±ST elevation), with <50% left anterior descending coronary artery stenosis and Thrombolysis in Myocardial Infarction flow grade ≥ 2 after percutaneous coronary intervention, were randomized 2:1:2 to once-daily AZD5718 200 mg or 50 mg, or placebo, in 4- and 12-week cohorts. Change in urine leukotriene E
RESULTS
Of 129 randomized patients, 128 received treatment (200 mg, n = 52; 50 mg, n = 25; placebo, n = 51). Statistically significant reductions in uLTE
CONCLUSIONS
In patients with recent myocardial infarction, AZD5718 was well tolerated, and leukotriene biosynthesis was dose-dependently inhibited. No significant changes in CFVR were detected.
CLINICALTRIALS
gov identifier: NCT03317002.

Identifiants

pubmed: 35842004
pii: S0167-5273(22)01084-1
doi: 10.1016/j.ijcard.2022.07.016
pii:
doi:

Substances chimiques

5-Lipoxygenase-Activating Protein Inhibitors 0
AZD5718 0
Pyrazoles 0

Banques de données

ClinicalTrials.gov
['NCT03317002']

Types de publication

Clinical Trial, Phase II Journal Article Randomized Controlled Trial

Langues

eng

Sous-ensembles de citation

IM

Pagination

34-40

Informations de copyright

Copyright © 2022 The Authors. Published by Elsevier B.V. All rights reserved.

Auteurs

Eva Prescott (E)

Department of Cardiology, Bispebjerg Hospital, University of Copenhagen, Copenhagen, Denmark. Electronic address: epre0004@regionh.dk.

Oskar Angerås (O)

Department of Molecular and Clinical Medicine, Sahlgrenska Academy, University of Gothenburg, and Department of Cardiology, Sahlgrenska University Hospital, Gothenburg, Sweden.

David Erlinge (D)

Cardiology, Department of Clinical Sciences, Lund University and Skåne University Hospital, Lund, Sweden.

Erik L Grove (EL)

Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark; Department of Clinical Medicine, Faculty of Health, Aarhus University, Aarhus, Denmark.

Marja Hedman (M)

Heart Center and Clinical Imaging Center, Kuopio University Hospital, Kuopio, Finland; Institute of Medicine, University of Eastern Finland, Kuopio, Finland.

Lisette O Jensen (LO)

Department of Cardiology, Odense University Hospital, Odense, Denmark.

John Pernow (J)

Division of Cardiology, Department of Medicine, Karolinska Institute, and Department of Cardiology, Karolinska University Hospital, Stockholm, Sweden.

Antti Saraste (A)

University of Turku and Heart Centre, Turku University Hospital, Turku, Finland.

Axel Åkerblom (A)

Department of Medical Sciences - Cardiology, and Uppsala Clinical Research Center, Uppsala University, Uppsala, Sweden.

Sara Svedlund (S)

Department of Clinical Physiology, Sahlgrenska University Hospital and Department of Molecular and Clinical Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.

Anna Rudvik (A)

Early Biometrics and Statistical Innovation, Data Science & AI, BioPharmaceuticals R&D, AstraZeneca, Gothenburg, Sweden.

Jane Knöchel (J)

Clinical Pharmacology and Quantitative Pharmacology, Clinical Pharmacology and Safety Sciences, BioPharmaceuticals R&D, AstraZeneca, Gothenburg, Sweden.

Eva-Lotte Lindstedt (EL)

Research and Early Clinical Development, Cardiovascular, Renal and Metabolic, BioPharmaceuticals R&D, AstraZeneca, Gothenburg, Sweden.

Pavlo Garkaviy (P)

Research and Early Clinical Development, Cardiovascular, Renal and Metabolic, BioPharmaceuticals R&D, AstraZeneca, Gothenburg, Sweden.

Li-Ming Gan (LM)

Department of Molecular and Clinical Medicine, Sahlgrenska Academy, University of Gothenburg, and Department of Cardiology, Sahlgrenska University Hospital, Gothenburg, Sweden; Research and Early Clinical Development, Cardiovascular, Renal and Metabolic, BioPharmaceuticals R&D, AstraZeneca, Gothenburg, Sweden.

Anders Gabrielsen (A)

Research and Early Clinical Development, Cardiovascular, Renal and Metabolic, BioPharmaceuticals R&D, AstraZeneca, Gothenburg, Sweden.

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Classifications MeSH